Figure 2 - uploaded by Naser Alsharairi
Content may be subject to copyright.
Role of dietary antioxidants against cigarette smoke-induced oxidative stress in lung cancer. (↓) decrease, (↑) increase.
Source publication
Smoking is considered a major risk factor in the development of lung diseases worldwide. Active smoking and secondhand (passive) smoke (SHS) are related to lung cancer (LC) risk. Oxidative stress (OS) and/or lipid peroxidation (LP) induced by cigarette smoke (CS) are found to be involved in the pathogenesis of LC. Meta-analyses and other case-contr...
Context in source publication
Similar publications
Objectives
There is accumulating evidence that lower socioeconomic groups are more exposed to secondhand smoke (SHS) than higher ones in the general population. The objective of the study was to examine the associations of education and income with SHS exposure among non-smoking pregnant women in Japan.
Methods
We analyzed data from 11,615 non-smo...
There is a population who is at such low risk of atherothrombotic disease that they do not need therapy. Low risk is determined by the absence of cigarette smoking, dyslipidemia, and hypertension. Dyslipidemia is defined as the Cholesterol retention fraction, which is defined as (LLD-c minus HDL-c)/ LDL-c. Hypertension is defined as a systolic bloo...
Citations
... Smoking induces carcinogenesis by causing metabolic changes at the DNA level, the formation of carcinogenic DNA adducts and will also lead to mutations. This will mainly cause the inhibition of genes such as p53 which is a tumor suppressor; and mutations in the Kirsten rat sarcoma viral oncogene homolog (KRAS) oncogene [53,54]. Smoking is considered a major risk factor in the development of lung disease worldwide. ...
According to recent data reported, it is noted that lung cancer is the leading cause of cancer death internationally followed by cardiovascular diseases and diabetes. This disease is observed in both women and men and is related to lifestyle habits. Several causes are reported to be at the origin of lung cancer, especially smoking. It is important to note that the majority of lung cancers develop in the bronchi, that is to say at the level of the upper airways which lead to the lungs, which does not however make it possible to rule out the risk factors that come under environmental pollution since man breathes the air quality of the environment every day for his breathing. This review of the literature has made it possible to draw up a state of knowledge in order to understand the risk factors that increase lung cancer. More specifically, this work will make it possible to raise awareness in the field of the fight against cancer, in particular lung cancer.
... They suggest that dietary habits may influence the lung cancer risk only in subjects that are, or have been, exposed to the carcinogens of the tobacco smoke. It is well known that smoking causes lung cancer in part through its pro-oxidant properties [56]. Therefore, it may be reasonable to assume that the "Healthy/prudent diet", with its high amounts of antioxidants, is more effective in preventing lung cancer in smokers and less effective in non-smokers. ...
The effect of dietary patterns on lung cancer risk is currently debated. In this study, we evaluated the association between different “a posteriori” dietary patterns and lung cancer risk. The search was carried out (February 2023) through Scopus, Web of Science, and PubMed databases. Meta-analysis was performed by a random-effects model using risk values (RR and OR) extracted from the 12 selected studies. Two main dietary patterns were identified and named “Western/meat” and “Healthy/prudent”. The highest adherence to the “Western/meat” dietary pattern significantly increased the lung cancer risk (OR = 1.39; 95% CI: 1.17–1.65; p = 0.0002) while the highest adherence to the “Healthy/prudent” pattern reduced it (OR = 0.65; 95% CI: 0.51–0.83; p = 0.001). A linear trend between both dietary patterns and lung cancer risk was observed. However, a statistically significant inverse dose–response trend was found only for the “Healthy/prudent” dietary pattern (regression coefficient = −0.0031, p = 0.003). Subgroup analyses showed that the “Western/meat” pattern significantly increased the lung cancer risk in former (n = 4) (OR = 1.93, 95% CI: 1.11–3.36) and current smokers (n = 7) (OR = 1.35, 95% CI: 1.06–1.71). Similarly, the “Healthy/prudent” pattern exerts a protective effect on former (n = 4) (OR = 0.61, 95% CI: 0.44–0.85) and current smokers (n = 8) (OR = 0.64, 95% CI: 0.46–0.88). For both dietary patterns, no significant effect was observed on never-smokers.
... The efficacy of dietary antioxidant intake in the treatment of NSCLC is also uncertain. Human and animal studies have demonstrated a beneficial effect of dietary vitamins (C, D, E, and carotenoids) and minerals (zinc and copper) intake in regards to NSCLC in smokers, while iron and retinol showed a detrimental effect [12]. Several randomized controlled trials (RCTs) of monoclonal antibody-based immunotherapy in combination with chemotherapeutic agents have shown promising therapeutic outcomes in patients with NSCLC [13]. ...
Flavonoids are the largest group of polyphenols, represented by many compounds that exhibit high anticancer properties. Quercetin (Q) and its main derivatives (rutin, quercitrin, isoquercitrin, isorhamnetin, tamarixetin, rhamnetin, and hyperoside) in the class of flavonols have been documented to exert anticancer activity. Q has been shown to be useful in the treatment of non-small cell lung cancer (NSCLC), as demonstrated by in vitro/in vivo studies, due to its antitumor, anti-inflammatory, anti-proliferative, anti-angiogenesis, and apoptotic properties. Some flavonoids
(flavone, anthocyanins, and proanthocyanidins) have been demonstrated to be effective in nicotineinduced NSCLC treatment. However, the molecular mechanisms of quercetin derivatives (QDs) in nicotine-induced NSCLC treatment remain unclear. Thus, this review aims to summarize the available literature on the therapeutic effects of QDs in nicotine-induced NSCLC.
... A recent review investigating the effects of dietary antioxidant intake on lung cancer (LC) risk among smokers and nonsmokers suggests that dietary vitamins (C, D, E, and carotenoids) and minerals (zinc and copper) may exert protective effects against cigarette smoke (CS)induced OS and/or inflammation. However, dietary retinol and iron intake did not provide any protection, and research suggests caution in recommending these for LC treatment [29]. There is a direct association between LC and asthma in smokers [30,31]. ...
Asthma is considered a chronic inflammatory disorder associated with airway hyperresponsiveness (AHR). Increased oxidative stress (OS) is a clinical feature of asthma, which promotes the inflammatory responses in bronchial/airway epithelial cells. Smokers and nonsmokers with asthma have been shown to have increases in several OS and inflammatory biomarkers. However, studies suggest significant differences in OS and inflammation biomarkers between smokers and nonsmokers. A few studies suggest associations between antioxidant intake from diet/supplements and asthma in patients with different smoking status. Evidence is lacking on the protective role of antioxidant vitamin and/or mineral consumption against asthma by smoking status with respect to inflammation and OS biomarkers. Therefore, the aim of this review is to highlight current knowledge regarding the relations between antioxidant intake, asthma, and its associated biomarkers, according to smoking status. This paper can be used to guide future research directions towards the health consequences of antioxidant intake in smoking and nonsmoking asthmatics.
... A recent review investigating the effects of dietary antioxidant intake on lung cancer (LC) risk among smokers and nonsmokers suggests that dietary vitamins (C, D, E and carotenoids) and minerals (zinc and copper) may exert protective effects against cigarette smoke (CS)induced OS and/or inflammation. However, dietary retinol and iron intake did not provide any protection, and research suggests caution in recommending these for LC treatment [27]. There is a direct association between LC and BA in smokers [28,29]. ...
Bronchial asthma (BA) is considered a chronic inflammatory disorder associated with airway hyperresponsiveness (AHR). Increased oxidative stress (OS) is a clinical feature of BA, which promotes the inflammatory responses in bronchial/airway epithelial cells. Smokers and nonsmokers with asthma have been shown to have increases in several OS and inflammatory biomarkers. A few studies suggest a relationship between antioxidant intake from diet/supplements and BA in smoking and nonsmoking asthmatics. Dietary carotenoids and vitamin C (VC) intake might reduce BA risk in smokers and/or non-smokers. Evidence is lacking on the protective role of antioxidant vitamin and/or mineral consumption against BA in smokers and nonsmokers with respect to inflammation and OS biomarkers. Therefore, the aim of this review is to highlight current knowledge regarding the relations between antioxidant intake, BA and its associated biomarkers in smokers and nonsmokers.
... A study of current smokers found a strong positive relationship between the levels of cotinine and its risk towards lung cancer. Former smokers as well as the never-smokers were found to have cotinine levels consistent with active smoking [164]. Cigarette smoking is associated with reduced incidence of EGFR mutations and serious adverse events. ...
Lung cancer (LC) is considered as one of the leading causes of cancer-associated mortalities. Cancer cells’ reprogrammed metabolism results in changes in metabolite concentrations, which can be utilized to identify a distinct metabolic pattern or fingerprint for cancer detection or diagnosis. By detecting different metabolic variations in the expression levels of LC patients, this will help and enhance early diagnosis methods as well as new treatment strategies. The majority of patients are identified at advanced stages after undergoing a number of surgical procedures or diagnostic testing, including the invasive procedures. This could be overcome by understanding the mechanism and function of differently regulated metabolites. Significant variations in the metabolites present in the different samples can be analyzed and used as early biomarkers. They could also be used to analyze the specific progression and type as well as stages of cancer type making it easier for the treatment process. The main aim of this review article is to focus on rewired metabolic pathways and the associated metabolite alterations that can be used as diagnostic and therapeutic targets in lung cancer diagnosis as well as treatment strategies.
... However, other studies suggest that b-carotene could induce lung cancer in smokers. Recent studies have shown the correlation between a diet rich in carotenoids and a diminishing risk of cardiovascular disease, cancer (b-carotene, lycopene), as well as ophthalmological diseases (lutein, zeaxanthin) (Alsharairi, 2022). ...
Background:
Lung cancer is a life-threatening disease that is still prevalent worldwide. This study aims to evaluate the effects of matricin, a sesquiterpene, on the carcinogenic agent benzo(a)pyrene [B(a)P]-induced lung cancer in Swiss albino mice.
Methods:
Lung cancer was induced by oral administration of B(a)P at 50 mg/kg b. wt. in model Swiss-albino mice (group II) as well in experimental group III, and treated with matricin (100 mg/kg b. wt.) in group III. Upon completion of treatment for 18 weeks, the changes in body weight, tumor formation, enzymatic and non-enzymatic antioxidant levels (GSH, SOD, GPx, GR, QR, CAT), lipid peroxidation (LPO) level, pro-inflammatory cytokines (TNF-α, IL-6, IL-1β), immunoglobulin levels (IgG, IgM), apoptosis markers (Bax, Bcl-xL), tumor markers (carcinoembryogenic antigen (CEA), neuron-specific enolase (NSE)), and histopathological (H&E) alterations were determined.
Results:
The results indicate that B(a)P caused a significant increase of tumor formation in the lungs, increased tumor markers and inflammatory cytokines in serum, and depletion of enzymatic/ non-enzymatic antioxidants and immunoglobulins, compared to the untreated control group. Matricin treatment significantly reversed the changes caused by B(a)P as evidenced by the biochemical and histopathological assays.
Conclusion:
The changes caused by matricin clearly indicate the cancer-preventive effects of matricin against B(a)P-induced lung cancer in animal models, which can be attributed to the antioxidant activity, immunomodulation, and mitigation of the NF-kβ pathway.
Cancer, a leading global cause of mortality, arises from intricate interactions between genetic and environmental factors, fueling uncontrolled cell growth. Amidst existing treatment limitations, vitamins have emerged as promising candidates for cancer prevention and treatment. This review focuses on Vitamins A, C, E, and D because of their protective activity against various types of cancer. They are essential as human metabolic coenzymes. Through a critical exploration of preclinical and clinical studies via PubMed and Google Scholar, the impact of these vitamins on cancer therapy was analyzed, unraveling their complicated mechanisms of action. Interestingly, vitamins impact immune function, antioxidant defense, inflammation, and epigenetic regulation, potentially enhancing outcomes by influencing cell behavior and countering stress and DNA damage. Encouraging clinical trial results have been observed; however, further well-controlled studies are imperative to validate their effectiveness, determine optimal dosages, and formulate comprehensive cancer prevention and treatment strategies. Personalized supplementation strategies, informed by medical expertise, are pivotal for optimal outcomes in both clinical and preclinical contexts. Nevertheless, conclusive evidence regarding the efficacy of vitamins in cancer prevention and treatment is still pending, urging further research and exploration in this compelling area of study.
